Review of cells overexpressing HAX 1 was AMN-107 Nilotinib significantly reduced and the cells depleted HAX 1 was compared fa erh ht In order to control much The respective negative. Furthermore, to determine whether a module HAX Chemosensitivit select t from EC9706, we treated 40 IN cisplatin into cells with different levels of expression of HAX 1 w. Remarkably, the mortality rate in cells overexpressing HAX 1 was reduced, but increased Ht into cells by a HAX respective negative controls Ersch Pft. These findings suggest that HAX f cell resistance EC9706 promotes the chemotherapy. HAX 1 f EC9706 promotes cell invasion, as n To search results, we examined the effect of modulation HAX 1 expression on EC9706 cell invasion. In vitro tests showed that overexpression of cell invasion HAX f Rderte the F Ability EC9706 cell invasion, compared to control cells pSinGFP/EC9706 On. In contrast, Ersch Pfung the HAX an inhibited cell invasion F Ability EC9706, compared to untreated cells and pLentiLox3.7/EC9706 EC9706 cells. These gains and losses of function experiments suggest that an invasion of HAX EC9706 cells f Promoted. HAX 1 f Promotes further growth of xenografts in vivo CCHS whether HAX tumorigenesis f of ESCC Promoted to investigate in vivo, we used a xenograft model mice bare M Where EC9706 cells were treated with different levels of expression, one of HAX injected subcutaneously. The results showed that Candesartan the volume and weight of the transplanted tumor showed a very good correlation with the H He HAX expression.
These data show that HAX promotes a feeder Lead cancer tumor growth in vivo f. HAX 1 regulates Pol B expression in vivo to achieve best Term, our in vitro determination HAX upregulation Pol expression in B cells CCHS, we the xenograft tumor tissues of EC9706 cells was derived and performed RT-PCR and immunohistochemical analysis, the expression of HAX study 1 and pol b. As expected, both mRNA and protein HAX 1 and Pol B in the tumor tissue of pSinGFP HAX 1/EC9706 cells compared to those of untreated or pSinGFP/EC9706 EC9706 derived upregulated cells. In contrast, both mRNA and protein HAX 1 and Pol B in the tumor tissue of pLentiLox3.7 siHAX 1/EC9706 cells compared to those reduced pLentiLox3.7/EC9706 cells derived. It is remarkable that we in the tumor tissue, the study looked at more strongTo r The functional HAX 1 in the progression of cancer of the feeder Hre looking for, we modulate HAX level in a cell line EC9706 and ECSS, the impact on the behavior of the b Sartigen cells. , The expression of lentiviral vector mediated RNAi an effective, stable gene silencing various biological systems and favors the characterization of gene functions in many cell types. Therefore, we have eukaryotic expression vector lentiviral pSinGFP HAX one and three lentiviral siRNA vectors pLentiLox3.7 siHAX 1239, 1408 pLentiLox3.7 siHAX built, and if pLentiLox3.7 HAX 1538th With the aid of these vectors has succeeded in stable cell lines, EC9706 HAX 1 to establish at different levels. Both RT-PCR and Western blot analysis best CONFIRMS overexpression or inactivation of Hax 1 in these cells. Interestingly, we observed a positive correlation between expression of Hax and Pol B expression in these cells.